ArticleJournal of the American Society of Nephrology : JASN2014
Administration of recombinant soluble urokinase receptor per se is not sufficient to induce podocyte alterations and proteinuria in mice.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 72 citations in OpenAlex.
- The role of suPAR and related proteins in kidney, heart diseases, and diabetes.The Journal of clinical investigation · 2026Review
- Serum Factors in Primary Podocytopathies.Antibodies (Basel, Switzerland) · 2025Review
- Association of soluble urokinase plasminogen activator receptor and epidermal growth factor with histopathological findings of kidney biopsy: a single-center study.BMC nephrology · 2025Article
- Prophylactic treatment of FSGS recurrence in patients who relapsed on a previous kidney graft.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Observational
- Pathogenesis of Focal Segmental Glomerulosclerosis and Related Disorders.Annual review of pathology · 2025Review
- suPAR: An Inflammatory Mediator for Kidneys.Kidney diseases (Basel, Switzerland) · 2022Review
- Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland) · 2021Review
- Biomarkers in pediatric glomerulonephritis and nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2021Review
- Immune-mediated entities of (primary) focal segmental glomerulosclerosis.Cell and tissue research · 2021Review
- Challenges in primary focal segmental glomerulosclerosis diagnosis: from the diagnostic algorithm to novel biomarkers.Clinical kidney journal · 2021Review
- suPAR, a Circulating Kidney Disease Factor.Frontiers in medicine · 2021Review
- Targeting the Urokinase-Type Plasminogen Activator Receptor (uPAR) in Human Diseases With a View to Non-invasive Imaging and Therapeutic Intervention.Frontiers in cell and developmental biology · 2021Review
- Nephrotic syndrome in a dish: recent developments in modeling in vitro.Pediatric nephrology (Berlin, Germany) · 2020Review
- Further Evidence That the Soluble Urokinase Plasminogen Activator Receptor Does Not Directly Injure Mice or Human Podocytes.Transplantation · 2020Article
- Autoimmunity in Focal Segmental Glomerulosclerosis: A Long-Standing Yet Elusive Association.Frontiers in medicine · 2020Review
- The Plasma Soluble Urokinase Plasminogen Activator Receptor Is Related to Disease Activity of Patients with ANCA-Associated Vasculitis.Mediators of inflammation · 2020Article
- C3a and suPAR drive versican V1 expression in tubular cells of focal segmental glomerulosclerosis.JCI insight · 2019Article
- c-Src is in the effector pathway linking uPAR and podocyte injury.The Journal of clinical investigation · 2019Article
- uPAR isoform 2 forms a dimer and induces severe kidney disease in mice.The Journal of clinical investigation · 2019Article
- MeSsAGe risk score: tool for renal biopsy decision in steroid-dependent nephrotic syndrome.Pediatric research · 2019Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circulating levels of soluble forms of urokinase-type plasminogen activator receptor (suPAR) are generally elevated in sera from children and adults with FSGS compared with levels in healthy persons or those with other types of kidney disease. In mice lacking the gene encoding uPAR, forced increases in suPAR concentration result in FSGS-like glomerular lesions and proteinuria. However, whether overexpression of suPAR, per se, contributes to the pathogenesis of FSGS in humans remains controversial. We conducted an independent set of animal experiments in which two different and well characterized forms of recombinant suPAR produced by eukaryotic cells were administered over the short or long term to wild-type (WT) mice. In accordance with the previous study, the delivered suPARs are deposited in the glomeruli. However, such deposition of either form of suPAR in the kidney did not result in increased glomerular proteinuria or altered podocyte architecture. Our findings suggest that glomerular deposits of suPAR caused by elevated plasma levels are not sufficient to engender albuminuria.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.